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Dr. Palatini misquotes our findings in his first sentence in that we do not mention the effects of heart rate (HR) reduction in our article (1). However, he then correctly describes our findings by pointing out that baseline HR did not affect the superiority of amlodipine-based versus atenolol-based therapy in the ASCOT-BPLA (Anglo-Scandinavian Cardiac Outcomes Trial–Blood Pressure Lowering Arm). He further misrepresents our findings when he says that in the ASCOT-BPLA “baseline HR was not predictive of outcome.” In fact, we reported that it predicted all-cause, noncardiovascular, and cardiovascular (CV) mortality, but not nonfatal CV events. These findings are compatible with our statement that “Baseline HR has been reported as a significant predictor of various CV outcomes in some but not all studies” (1). We believe that the data regarding predictability of HR are less consistent than Dr. Palatini suggests, as witnessed by the study that we referenced (2) and a more recent publication (3). We acknowledge that in studies of secondary prevention (e.g., the INVEST [INternational VErapamil-SR/trandolapril STudy]) (4), HR is a more consistent predictor of cardiovascular outcomes, but patients with coronary heart disease were excluded from the ASCOT study.

We are unaware of any published data describing “problems” of HR measurement using semiautomatic blood pressure devices.

We are urged to report the association between “final HR” and CV outcomes. We briefly reported that associations with attained HR at 6 weeks post-randomization (almost all in-trial HR changes had occurred by then) were apparent with coronary but not other end points. In an earlier publication, we reported the impact on CV events of the “final” and accumulated mean levels of various parameters including HR (5). In general, accumulated mean levels were better predictors of CV events. Higher HR was apparently beneficial in terms of CV outcomes, but this was presumably confounded by the disadvantages of the atenolol-based regimen.

However, we did not focus on the variable predictability of HR because that was not the purpose of the study. We wanted to know whether having a higher baseline HR attenuated the superior effects on major CV events of the amlodipine-based compared with atenolol-based regimen. We could find no evidence of any such attenuation, and hence we believe that an increased baseline HR should not be an indication for preferential use of beta-blockade in hypertensive populations without coronary heart disease. Even if baseline HR had not predicted CV outcomes in the ASCOT study, we believe that the same conclusion should be drawn.

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